Selective atrial vagal denervation guided by spectral mapping to treat advanced atrioventricular block.

AIMS: Asymptomatic nocturnal long ventricular pauses are usually detected accidentally and it has been suggested that they may lead to sudden death. Identification of predisposing factors could prevent cardiovascular events. METHODS AND RESULTS: We report the case of a patient with frequent asymptomatic nocturnal ventricular pauses of 3-11 s, characteristic of a vagally mediated atrioventricular (AV) block. Echocardiography, treadmill test, thyroid function test levels, and polysomnogram were normal. In an attempt to reduce the risk, it was decided that an atrial vagal denervation induced by radiofrequency (RF) ablation (cardioneuroablation) could be useful. Spectral mapping was used to localize endocardial vagal innervation in the right and left aspects of the inter-atrial septum, responsible for the sinus node and AV node modulation, and RF pulses were applied in those sites only. After finishing the procedure, significant changes were observed in the heart rate (66-90 b.p.m.), atrial-His interval (115-74 ms), Wenckebach cycle length (820-570 ms), and sinus node recovery time (1100-760 ms). Follow-up Holter recording demonstrated that the number of ventricular pauses had reduced from 438 to 0. Heart rate and time domain characteristics were compatible with vagal denervation. CONCLUSION: Ablation of the endocardial vagal innervation sites seems to be safe and efficient in reducing the frequency and the length of the ventricular pauses. It was possible by identifying certain spectral components of the atrial electrogram, resulting in a conservative approach.

Sympathetic nerve stimulation, not circulating norepinephrine, modulates T-peak to T-end interval by increasing global dispersion of repolarization.

BACKGROUND: T-peak to T-end interval (Tp-e) is an independent marker of sudden cardiac death. Modulation of Tp-e by sympathetic nerve activation and circulating norepinephrine is not well understood. The purpose of this study was to characterize endocardial and epicardial dispersion of repolarization (DOR) and its effects on Tp-e with sympathetic activation. METHODS AND RESULTS: In Yorkshire pigs (n=13), a sternotomy was performed and the heart and bilateral stellate ganglia were exposed. A 56-electrode sock and 64-electrode basket catheter were placed around the epicardium and in the left ventricle (LV), respectively. Activation recovery interval, DOR, defined as variance in repolarization time, and Tp-e were assessed before and after left, right, and bilateral stellate ganglia stimulation and norepinephrine infusion. LV endocardial and epicardial activation recovery intervals significantly decreased, and LV endocardial and epicardial DOR increased during sympathetic nerve stimulation. There were no LV epicardial versus endocardial differences in activation recovery interval during sympathetic stimulation, and regional endocardial activation recovery interval patterns were similar to the epicardium. Tp-e prolonged during left (from 40.4±2.2 ms to 92.4±12.4 ms; P<0.01), right (from 47.7±2.6 ms to 80.7±11.5 ms; P<0.01), and bilateral (from 47.5±2.8 ms to 78.1±9.8 ms; P<0.01) stellate stimulation and strongly correlated with whole heart DOR during stimulation (P<0.001, R=0.86). Of note, norepinephrine infusion did not increase DOR or Tp-e. CONCLUSIONS: Regional patterns of LV endocardial sympathetic innervation are similar to that of LV epicardium. Tp-e correlated with whole heart DOR during sympathetic nerve activation. Circulating norepinephrine did not affect DOR or Tp-e.

Electrophysiological effects of right and left vagal nerve stimulation on the ventricular myocardium.

Vagal nerve stimulation (VNS) has been proposed as a cardioprotective intervention. However, regional ventricular electrophysiological effects of VNS are not well characterized. The purpose of this study was to evaluate effects of right and left VNS on electrophysiological properties of the ventricles and hemodynamic parameters. In Yorkshire pigs, a 56-electrode sock was used for epicardial (n = 12) activation recovery interval (ARI) recordings and a 64-electrode catheter for endocardial (n = 9) ARI recordings at baseline and during VNS. Hemodynamic recordings were obtained using a conductance catheter. Right and left VNS decreased heart rate (84 ± 5 to 71 ± 5 beats/min and 84 ± 4 to 73 ± 5 beats/min), left ventricular pressure (89 ± 9 to 77 ± 9 mmHg and 91 ± 9 to 83 ± 9 mmHg), and dP/dtmax (1,660 ± 154 to 1,490 ± 160 mmHg/s and 1,595 ± 155 to 1,416 ± 134 mmHg/s) and prolonged ARI (327 ± 18 to 350 ± 23 ms and 327 ± 16 to 347 ± 21 ms, P < 0.05 vs. baseline for all parameters and P = not significant for right VNS vs. left VNS). No anterior-posterior-lateral regional differences in the prolongation of ARI during right or left VNS were found. However, endocardial ARI prolonged more than epicardial ARI, and apical ARI prolonged more than basal ARI during both right and left VNS. Changes in dP/dtmax showed the strongest correlation with ventricular ARI effects (R(2) = 0.81, P < 0.0001) than either heart rate (R(2) = 0.58, P < 0.01) or left ventricular pressure (R(2) = 0.52, P < 0.05). Therefore, right and left VNS have similar effects on ventricular ARI, in contrast to sympathetic stimulation, which shows regional differences. The decrease in inotropy correlates best with ventricular electrophysiological effects.

Endocardial autonomic denervation of the left atrium to treat vasovagal syncope: an early experience in humans.

BACKGROUND: Vasovagal syncope (VVS) is the most common cause of recurrent syncope that can be debilitating despite optimal conventional therapy. The aim of this study was to evaluate the feasibility and efficacy of selective endocardial autonomic denervation in left atrium (LA) as an alternative treatment strategy in patients with highly symptomatic VVS. METHODS AND RESULTS: Ten consecutive patients (mean age, 50.4±6.4 years; 7 women) with a medium of 3.5 (range, 2-20) recurrent episodes of VVS during the preceding year and positive head-up tilt testing in whom standard therapies were ineffective or poorly tolerated were enrolled. Ganglionated plexi (GP) in the LA, identified by high-frequency stimulation, was targeted by radiofrequency catheter ablation. The patients were then followed up at 3, 6, 12, 24, and 36 months, including repeated head-up tilt testing and Holter at 3 and 12 months. Radiofrequency energy was applied at the left superior GP in 10 patients, right anterior GP in 5, and left inferior GP in 3, using an 8-mm ablation catheter. Vagal response, defined as transient ventricular asystole, atrioventricular block, or an increase in R-R interval by 50%, was observed during ablation in all GP sites. The end point of procedure was the inhibition of the vagal response at target sites. At 30±16 (range, 13-55) months of follow-up, no patient had any recurrence of syncope and all patients had significant improvement in symptoms, but 5 of 10 patients reported transient prodromes. No complications occurred. CONCLUSIONS: Comprehensive endocardial autonomic denervation of the LA demonstrates the feasibility of treating VVS in medium-term follow-up.

Prenatal development of the human epicardiac Ganglia.

The aim of this study was to determine the developmental anatomy of intrinsic cardiac ganglia with respect to epicardiac ganglionated nerve plexus in the human fetuses at different gestation stages. Twenty fetal hearts were investigated applying a technique of histochemistry for acetylcholinesterase to visualize the epicardiac neural ganglionated plexus with its subsequent examinations on total (non-sectioned) hearts. Most epicardiac ganglia embodied multilayered neurons and were oval in shape, but some ganglia involved neurons lying in one layer or had the irregular appearance because of their extensions along inter-ganglionic nerves. The mean ganglion area of fetuses at gestation stages of 15-40 weeks was 0.03 +/- 0.008 mm(2). The largest epicardiac ganglia, reaching in area 0.4 mm(2), were concentrated on the dorsal surface of both atria. The particular fused or "dual" ganglia were identified at the gestation stages of 23-40 weeks, but they composed only 2.3 +/- 0.7% of all found epicardiac ganglia. A direct positive correlation was determined between the fetal age and the ganglion area (mm(2)) as well as between the fetal age and the number of inter-ganglionic nerves. The revealed appearance of epicardiac ganglia in the human fetuses at 15-40 weeks of gestation confirms their prenatal development and presumable intrinsic remodelling.

Evaluation of catheter ablation of periatrial ganglionic plexi in patients with atrial fibrillation.

Recent data suggests that the cardiac autonomic nervous system has an important role in the initiation and maintenance of atrial fibrillation (AF). This study investigated (1) the feasibility of identifying and targeting these autonomic ganglia using endocardial radiofrequency stimulation and ablation, respectively; (2) the efficacy of endocardial ablation to completely eliminate the vagal response elicited from epicardial stimulation; and (3) the effect of autonomic ablation on the acute inducibility of AF. The study included 18 patients referred for catheter ablation of suspected vagal-mediated AF. The endocardial left atrial surface was stimulated at high frequency (20 to 50 Hz) to elicit a vagal response. In selected patients (n = 5), pericardial access was obtained using a subxyphoid puncture to permit epicardial stimulation. Catheter ablation of the putative autonomic ganglionic sites was performed from the left atrial endocardium using irrigated radiofrequency energy. After ablation of all identifiable autonomic ganglia, high-frequency pacing was repeated to induce AF. In all patients, stimulation at certain endocardial sites elicited a vagal response. Endocardial ablation abrogated this vagal responsiveness. Furthermore, for sites accessible from the pericardium, the vagal response elicited using epicardial stimulation was also eliminated. Despite successful ablation of these ganglia, AF was still inducible in 17 of 18 patients. In conclusion, successful ablation of autonomic ganglia from an endocardial approach can be reliably achieved using an irrigated catheter. In addition, ablation of these structures in patients with vagal-mediated AF is insufficient to prevent its acute reinduction with high-frequency atrial stimulation.

Biventricular ICD implant using endocardial LV lead placement from the left subclavian vein approach and transseptal puncture via the transfemoral route.

We present the case of a 72 years old diabetic male patient with severe dilated ischaemic cardiomyopathy and New York Heart Association functional class III symptoms and previous unsuccessful attempts to cardiac resynchronization therapy using the conventional epicardial left ventricular (LV) pacing through the coronary sinus. He also had an indication for ICD implantation. We successfully implanted a biventricular ICD system from the standard left subclavian vein approach using endocardial placement of the LV lead via a transfemorally performed transeptal puncture. This technique offered him a suitable alternative to either a thoracoscopic LV lead placement (not routinely performed in our centre) or a high-risk thoracotomy procedure and multisite pacing using epicardial leads.

Transmural and endocardial Purkinje activation in pigs before local myocardial activation after defibrillation shocks.

BACKGROUND: Earliest recorded postshock myocardial activations in pigs originate in the subepicardium of the apex and lateral free wall of the left ventricle (LV) 30-90 ms after the shock. OBJECTIVE: The purpose of this study was to determine whether the Purkinje system is a candidate for the source of postshock activations by performing endocardial and transmural postshock activation mapping. METHODS: In five pigs, 32 plunge needles with 12 electrodes (1-mm spacing) were inserted into the LV apex and lateral free wall. Up to 70 plunge needles with six electrodes (2-mm spacing) were spread throughout the remainder of the LV, while 9-12 plunge needles with four electrodes (2-mm spacing) were inserted into the right ventricle. A basket catheter with 32 bipolar recording sites was inserted into the LV. Defibrillation-threshold (DFT)-level shocks were delivered during 10 episodes of electrically induced ventricular fibrillation. Electrograms of postshock activation cycles were analyzed for Purkinje and myocardial activations. RESULTS: Purkinje activations were recorded before local myocardial activation in 9% of basket electrograms and in 15% of plunge needles during the first postshock activation cycle. Purkinje activations were identified during the first and subsequent several postshock activation cycles in at least one basket and one needle electrogram in 96% and 98% of defibrillation episodes, respectively. CONCLUSIONS: The Purkinje system is active during the early postshock activation cycles after DFT-level shocks. Further studies are required to determine whether activation initiates in the Purkinje system or whether it is activated by the myocardium or by Purkinje-myocardial junctional cells.

Effects of carvedilol on M2 receptors and cholinesterase-positive nerves in adriamycin-induced rat failing heart.

Heart failure is correlated with attenuation of parasympathetic nervous function and enhanced sympathetic activity. Carvedilol, a third-generation beta-blocker, may improve the prognosis of heart failure better than selective beta(1)-blockers. Not all of its effects, however, can be explained by direct actions on the sympathetic nervous system. This study was therefore performed to investigate the possible alterations of muscarinic cholinergic (M)(2) receptors and cholinesterase-positive nerves in different regions of the adriamycin-induced failing rat heart, and the potential effects of carvedilol on these M(2) receptors and cholinesterase-positive nerves. Karnovsky-Roots histochemical staining combined with point counting methods, and immunochemical streptavidin-biotin complex staining and image analysis were used to test the distribution of cholinesterase-positive nerves and the expression of M(2) receptors, respectively. Our results show that the cholinesterase-positive nerve system was downregulated in the adriamycin-induced failing heart group, while the density of M(2) receptors was increased in the carvedilol 3- and 10-mg/kg body weight groups, especially in the endocardial tissues of the left-ventricular free wall. It is concluded that upregulation of M(2) receptors may be one of the potential mechanisms by which carvedilol exert its action on heart failure.

Feasibility study of endocardial mapping of ganglionated plexuses during catheter ablation of atrial fibrillation.

BACKGROUND: Numerous reports have demonstrated an association between autonomic tone and atrial fibrillation (AF). Pulmonary vein (PV) denervation during catheter ablation of AF has been shown to significantly reduce recurrence of AF. OBJECTIVES: The purpose of this study was to assess the safety and efficacy of high-frequency stimulation at mapping cardiac ganglionated plexuses in patients undergoing catheter ablation of AF. METHODS: Fourteen patients with a history of symptomatic AF underwent a single transseptal approach and electroanatomic mapping of the left atrium, right atrium, and coronary sinus. Using high-frequency stimulation with patients under general anesthesia (20-50 Hz, 5-15 V, pulse width 10 ms), mapping of ganglionated plexuses was performed. Radiofrequency (RF) ablation was performed during AF guided by complex fractionated atrial electrograms. Lesions were mostly delivered circumferentially in the antral area of the PVs, predominantly over and adjacent to regions of ganglionated plexuses. RESULTS: There was a mean of 4 +/- 1 (range 2-6) ganglionated plexuses per patient, and a mean total of 3 +/- 1 RF applications were delivered over positive vagal sites. Although a vagal response occurred infrequently during ablation (0.9%), postablation high-frequency stimulation failed to provoke a vagal response in 30 (88%) of 34 previously positive vagal sites that underwent ablation. CONCLUSION: Ganglionated plexuses can be precisely mapped using high-frequency stimulation and are located predominantly in the path of lesions delivered during ablation of AF. Objective documentation of modification of autonomic tone can be documented in the majority of patients. Future studies are required to determine the specific role of mapping and targeting of ganglionated plexuses in patients undergoing catheter ablation of AF.

Effect of autonomic nervous system on the transmural dispersion of ventricular repolarization in intact canine.

The effect of the autonomic nerves on the transmural dispersion of ventricular repolarization in intact canine was investigated. By using the monophasic action potential (MAP) recording technique, monophasic action potentials (MAPs) of the epicardium (Epi), midmyocardium (Mid) and endocardium (Endo) were recorded simultaneously by specially designed plunge-needle electrodes at the left ventricular free wall in 12 open-chest dogs. MAPD90 and transmural dispersion of repolarization among three myocardial layers as well as the incidence of the EAD before autonomic nervous stimulation and during autonomic nervous stimulation were compared. The results showed that the MAPD90 of Epi, Mid and Endo before autonomic nervous stimulation were 278 +/- 11 ms, 316 +/- 16 ms and 270 +/- 12 ms respectively, the MAPD90 of Mid was significantly longer than that of Epi or Endo (P<0.01). MAPD90 of Epi, Mid and Endo were shortened by 19 +/- 4 ms, 45 +/- 6 ms, 18 +/- 3 ms respectively during sympathetic stimulation. Compared with that of the control, the transmural dispersion of repolarization during sympathetic stimulation was shortened from 44 +/- 4 ms to 15 +/- 3 ms (P<0.01), but early afterdepolarizations were elicited in the Mid of 5 dogs (41%) during sympathetic stimulation. Parasympathetic stimulation did not significantly affect the MAPD90 in the three layers. It is concluded that there is the transmural dispersion of ventricular repolarization in intact canine. Sympathetic stimulation can reduce transmural dispersion of repolarization, but it can produce early afterdepolarizations in the Mid. Parasympathetic stimulation does not significantly affect the transmural dispersion of ventricular repolarization.

Effect of autonomic nervous system on the transmural dispersion of ventricular repolarization in intact canine / 华中科技大学学报（医学）（英德文版）

The effect of the autonomic nerves on the transmural dispersion of ventricular repolarization in intact canine was investigated. By using the monophasic action potential (MAP) recording technique, monophasic action potentials (MAPs) of the epicardium (Epi), midmyocardium (Mid) and endocardium (Endo) were recorded simultaneously by specially designed plunge-needle electrodes at the left ventricular free wall in 12 open-chest dogs. MAPD90 and transmural dispersion of repolarization among three myocardial layers as well as the incidence of the EAD before autonomic nervous stimulation and during autonomic nervous stimulation were compared. The results showed that the MAPD90 of Epi, Mid and Endo before autonomic nervous stimulation were 278 +/- 11 ms, 316 +/- 16 ms and 270 +/- 12 ms respectively, the MAPD90 of Mid was significantly longer than that of Epi or Endo (P<0.01). MAPD90 of Epi, Mid and Endo were shortened by 19 +/- 4 ms, 45 +/- 6 ms, 18 +/- 3 ms respectively during sympathetic stimulation. Compared with that of the control, the transmural dispersion of repolarization during sympathetic stimulation was shortened from 44 +/- 4 ms to 15 +/- 3 ms (P<0.01), but early afterdepolarizations were elicited in the Mid of 5 dogs (41%) during sympathetic stimulation. Parasympathetic stimulation did not significantly affect the MAPD90 in the three layers. It is concluded that there is the transmural dispersion of ventricular repolarization in intact canine. Sympathetic stimulation can reduce transmural dispersion of repolarization, but it can produce early afterdepolarizations in the Mid. Parasympathetic stimulation does not significantly affect the transmural dispersion of ventricular repolarization.

Distribution of cardiac nerves in patients with diabetes mellitus: an immunohistochemical postmortem study of human hearts.

BACKGROUND: Autonomic neuropathy and functional cardiac denervation are complications of diabetes mellitus (DM). It is unknown if DM patients show histopathologic evidence of cardiac denervation. METHODS AND RESULTS: Nine sites were sampled at fixed distances from the atrioventricular valves from 27 postmortem hearts. Sections were stained with antibodies to S100 protein and to neurofilament (NF). Samples were visualized by light microscopy using the avidin-biotin peroxidase technique. The amount of cardiac nerves was graded blindly using semiquantitative methods according to the following criteria: Grade 0=presence of nerves in the epicardium only; Grade 1=strictly perivascular nerves; Grade 2=Grade 1 and nerve sprouts between myocardial cells sporadically; Grade 3=Grade 2 and nerve sprouts throughout the myocardium and endocardium. Specimens were divided into four groups. Control group consisted of patients with neither myocardial infarction (MI) nor DM. Experimental groups consisted of MI (n=7), MI with DM (n=6), and DM without MI (n=8). Average age of all patients was 57.3+/-15.7 years. No age differences existed among groups. Heterogeneous nerve distribution existed in all groups. S100-positive nerve density for control, MI, DM and MI, and DM without MI are 1.95+/-0.40, 1.66+/-0.54, 1.54+/-0.37, and 1.81+/-0.14, respectively (P=ns). NF-positive nerve density in the same groups were 1.10+/-0.18, 1.31+/-0.24, 1.13+/-0.12, and 1.19+/-0.42, respectively (P=ns). No differences in nerve densities between anterior and inferoposterior sections of the left ventricle existed. CONCLUSION: In postmortem human hearts, cardiac nerve distribution was heterogeneous among normal, MI, and DM patients. No evidence of cardiac denervation in patients with DM was demonstrated.

Localisation and quantitation of autonomic innervation in the porcine heart II: endocardium, myocardium and epicardium.

The immunological problems of pig hearts supporting life in human recipients have potentially been solved by transgenic technology. Nevertheless, other problems still remain. Autonomic innervation is important for the control of cardiac dynamics and there is evidence suggesting that some neurons remain intact after transplantation. Previous studies in the human heart have established regional differences in both general autonomic innervation and in its component neural subpopulations. Such studies are lacking in the pig heart. Quantitative immunohistochemical and histochemical techniques were used to demonstrate the pattern of innervation in pig hearts (Sus scrofa). Gradients of immunoreactivity for the general neural marker protein gene product 9.5 were observed both within and between the endocardial, myocardial and epicardial plexuses throughout the 4 cardiac chambers. An extensive ganglionated plexus was observed in the epicardial tissues and, to a lesser extent, in the myocardial tissues. The predominant neural subpopulation displayed acetylcholinesterase activity, throughout the endocardium, myocardium and epicardium. These nerves showed a right to left gradient in density in the endocardial plexus, which was not observed in either the myocardial or epicardial plexuses. A large proportion of nerves in the ganglionated plexus of the atrial epicardial tissues displayed AChE activity, together with their cell bodies. Tyrosine hydroxylase (TH)-immunoreactive nerves were the next most prominent subpopulation throughout the heart. TH-immunoreactive cell bodies were observed in the atrial ganglionated plexuses. Endocardial TH- and NPY-immunoreactive nerves also displayed a right to left gradient in density, whereas in the epicardial tissues they showed a ventricular to atrial gradient. Calcitonin gene-related peptide (CGRP)-immunoreactive nerves were the most abundant peptide-containing subpopulation after those possessing NPY immunoreactivity. They were most abundant in the epicardial tissues of the ventricles. Several important differences were observed between the innervation of the pig heart compared with the human heart. These differences may have implications for the function of donor transgenic pig hearts within human recipients.

The autonomic control of the transmural dispersion of ventricular repolarization in anesthetized dogs.

INTRODUCTION: The initiation of ventricular arrhythmias is in part associated with autonomic nervous tone. We investigated the effects of sympathetic and parasympathetic stimulation on the monophasic action potentials (MAPs) of the epicardium (EPi), mid-myocardial (M) region, and endocardium (Endo) in vivo. METHODS AND RESULTS: In 12 mongrel open chest anesthetized dogs, both sides of the cervical vagus nerves and stellate ganglia were crushed with a tight ligature. Right atrial pacing at 600 msec cycle length was begun after the sinus nodal area had been crushed. MAPs from the M region were measured by two needle electrodes that were supported by a W-shaped plastic frame. The epicardial, M region, and endocardial MAP durations at 90% repolarization (MAPD90) were 287+/-7, 315+/-7, and 290+/-8 msec, respectively. The MAPD90 from M cells was longer than that from Epi or Endo. Sympathetic stimulation shortened MAPD90 more in the M region (53+/-4 msec) than that in the Epi (27+/-3 msec) or Endo (26+/-4 msec). The transmural dispersion of repolarization during sympathetic stimulation was shorter than that of the control. Parasympathetic stimulation did not significantly affect any of the MAPD90 values. Simultaneous sympathetic and parasympathetic stimulation produced changes not significantly to those produced by sympathetic stimulation alone. CONCLUSION: Our results suggest that sympathetic activity can reduce transmural dispersion of repolarization under autonomic control in the canine heart under baseline conditions.

Localization of precise origin of idiopathic ventricular tachycardia from the right ventricular outflow tract by a 12-lead ECG: a study of pace mapping using a multielectrode "basket" catheter.

Radiofrequency catheter ablation guided by pace-mapping techniques has proven effective in eliminating idiopathic ventricular tachycardia (VT) originating from the right ventricular outflow tract (RVOT). A method for rapidly identifying the origin of VT from 12-lead electrocardiogram (ECG) findings would be helpful for the catheter ablation procedure. The purpose of this study is to precisely localize the origin of idiopathic VT from the RVOT by a 12-lead ECG from a study of multipoint pace mapping. In one patient with premature ventricular complex (PVC) and 3 with VT, a "basket" catheter was deployed in the RVOT for bipolar pacing from 56 sites in the endocardium of RVOT. Under fluoroscopy the pacing sites were classified into the septum and free wall. We investigated the QRS morphology in leads, I, II, and III; the depth of the QS wave in leads aVR and aVL; and the height of the initial r wave in leads V1 and V2. Pacing was captured in 30-47 of 56 sites (54%-84%). As the pacing sites changed from the anterior to posterior of the septum, the QS notch (-) type in lead I shifted through rs to R, while a shift from R type to rR' or Rr' was noted in leads II and III. As the pacing sites changed from the anterior to posterior of the free wall, lead I showed a shift from the QS notch (+) type to R, while a shift from rR' to Rr' (or rR' unchanged) was found in leads II and III. The depth of the QS wave in leads aVR and aVL showed a tendency for aVR to be deeper than aVL toward the posterolateral attachment of both the septum and free wall, whereas aVL tended to be deeper than aVR toward the anterior attachment. The initial r waves in V1 and V2 became greater as the pacing site was positioned at a higher or more posterior location. These findings may provide more precise and clinically useful diagnostic information on the site of the origin of idiopathic VT originating from the RVOT by a 12-lead ECG.

Uncommon atrial flutter: characteristics, mechanisms, and results of ablative therapy.

Thirty-seven patients with atrial flutter were studied with catheter mapping and radiofrequency ablation. Uncommon atrial flutter occurred in 20 out of 37 (54%) patients. Atrial endocardial mapping showed two types of uncommon atrial flutter. In 15 patients (group I) it was characterized by a single clockwise circuit whereas in 5 patients (Group II) it was characterized by the presence of more than one circuit and/or localized atrial fibrillation. RFA ablation was acutely successful in 14 out of 15 patients (93%) in Group I and in 2 out of 5 (40%) patients in Group II. On long-term follow-up a significantly larger number of patients in Group I versus Group II (86% vs 20%) remained free of atrial flutter recurrence. We conclude that uncommon atrial flutter is a heterogeneous entity involving one or more reentrant circuits. Uncommon atrial flutter with multiple circuits may not be suitable for RFA.